Burns pt 1 Flashcards

1
Q

What are the 2 major causes of death in burn patients?

A

Multiple organ failure and infection

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2
Q

How are burn injuries classified?

A

Burn injuries, regardless of their etiology, are classified according to the depth and extent of skin and tissue destruction, as well as the Total Burn Surface Area (TBSA) involved.

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3
Q

What are First Degree Burns?

A

First-degree (superficial) burns are limited to the epidermis, the outermost layer of skin. Think sunburn.

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4
Q

What are Second Degree Burns?

A

Second-degree burns, also known as deep and superficial partial-thickness burns, extend to the dermis.

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5
Q

What are Third Degree Burns?

A

Third-degree burns, or full-thickness burns, extend to the subcutaneous tissue lying below the dermis. The entire skin thickness is destroyed with third-degree burns.

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6
Q

What are Fourth Degree Burns?

A

A fourth-degree burn classification is used by some to describe structures burned below the dermis, such as muscle, fascia, and bone. (more seen with electrical injuries)

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7
Q

What does the Rule of Nines calculate?

A

The severity based on the amount of surface area covered in second and third-degree burns.

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8
Q

What is the percentage associated with the arms, head, legs, and torso?

A

Arms - 9%
Head - 10%
Legs - 18%
Torso - 36%

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9
Q

What is a Major Burn?

A

-A second-degree burn involving more than 10% of the TBSA in adults or 20% at extremes of age
-A third-degree burn involving more than 10% of the TBSA in adults
-Any electrical burn
-A burn complicated by smoke inhalation.

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10
Q

What are the 4 types of burn injuries?

A

-Thermal
-Electrical
-Chemical
-Inhalation

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11
Q

Describe Thermal Burns

A

(43% flame, 34% scald, 9% contact, 7% other)
-Commonly occur in/around the home
-Scald injuries predominantly children

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12
Q

Describe electrical burns

A

-Extent of burn depends on amount of thermal energy conducted through the skin
-10-46% cardiac arrhythmias and myocardial damage
-Severe damage to bones, blood vessels, muscle and nerves
-Myoglobinemia increased risk of renal failure

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13
Q

Describe Chemical burns

A

-Commonly occur in a laboratory/industrial setting
-Skin disruption continues until irritant is removed/neutralized
-Initial Tx: application of copious amount of water or NS irrigation

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14
Q

Describe Inhalation burns

A

-Often accompany a thermal burn, airway damage can vary
-Classification based on anatomic location:
Upper-airway, lower-airway, and metabolic asphyxiation. All 3 types may coexist in the burn patient.

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15
Q

What are the warning signs of respiratory injury?

A

-hoarseness
-sore throat
-dysphagia
-hemoptysis
-tachypnea
-the use of accessory muscles
-wheezing
-carbonaceous sputum
-elevated carbon monoxide levels
-Observance of soot around nose/mouth

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16
Q

What is the biphasic organ response to burn injury?

A

The treatment of the burn patient will evolve as they progress through the early resuscitative phase to the later hypermetabolic state.
-Early changes and later changes differ based on organ system

17
Q

What are the early changes associated with organ response to burn injury?

A

-CV: Shock
-U: Oliguria
-GI: Ileus
-MSK: Hypoperfusion
-Pulm: Hypoventilation
-Endo: Catabolism
-Immuno: Inflammation (SIRS)
-CNS: Agitation

18
Q

What are the Late changes associated with organ response to burn injury?

A

-CV: Hyperdynamic
-U: Diuresis
-GI: Hypermotility
-MSK: Hyperperfusion
-Pulm: Hyperventilation
-Endo: Anabolism
-Immuno: Suppression
-CNS: Obtundation

19
Q

What are the 3 phases of management of the burn patient?

A

-Resuscitative Phase
-Burn Management: Debridement & Grafting
-Reconstructive Phase

20
Q

What is the goal of burn therapy?

A

The goal of burn therapy is to rapidly restore skin integrity.

21
Q

What are the pulmonary changes associated with burns?

A

-Decreased FRC and Chest wall compliance if chest wall burned
-Fluid shifts, interstitial edema, release of inflammatory mediators = pulmonary edema
-Significant a-A Gradient increases (Minute Ventilation increases to 40 L/min from normal 6 L/min)
-CXR normal in early phase progressing to pulmonary edema

22
Q

Why is the burned patient at risk for Pulmonary Edema?

A

-Impaired vascular/capillary permeability combined with fluid resuscitation
-Mechanical ventilation often required especially with concomitant inhalation injury

23
Q

What is important to know regarding ALI & ARDS and the burned patient?

A

-Acute onset of impaired oxygen exchange; partial pressure of arterial oxygen/fraction of inspired oxygen (Pa o 2 /Fi o 2) ratio of less than 300.
-Increased risk M&M due to respiratory failure, hypoxia, multiorgan failure, and pneumonia

24
Q

What are ventilation strategies to use in the burned patient?

A

-Low-volume lung protective ventilation reduces overinflation and barotrauma
-Use ideal body weight
-PEEP
-Modest permissive hypercapnia
-Nonconventional and high-frequency oscillatory modes of ventilation

25
Q

What is the gold standard for airway eval in the burned patient?

A

Fiberoptic bronchoscope is the gold standard!

26
Q

What is the treatment of upper airway injury?

A

Early endotracheal intubation secondary to glottic/facial edema worsening with resuscitation.

27
Q

Which patients are at risk for airway damage?

A

Involving a fire that occurred in a closed space or the development of unconsciousness or stupor that prevented the patient from protecting their airway

28
Q

How does injury differ above the oropharynx vs below the vocal cords?

A

Above the oropharynx: thermal injury produces inflammation that can occlude airway.

Below VC: damage is due to soot/chemicals (heat dissipates by this point).

29
Q

Why do you avoid the use of Succinylcholine > 24 hours after burn injury?

A

-Ach receptor up-regulation occurs after burn injury
-Succ releases K+ = possible cardiac arrest

30
Q

How does Carbon Monoxide cause its effects?

A

Binds to Hgb with 200 times greater affinity than O2.
-50-60% fire victims die from CO poisoning

31
Q

What are the S/Sx of Carbon Monoxide poisoning?

A

-Metabolic acidosis
-Oxy-Hgb dissociation curve LEFT
-Dec O2 content on ABG
-Falsely elevated SpO2 reading (pulse ox doesn’t detect CO)

32
Q

How do you diagnose CO poisoning?

A

COHgb levels using a laboratory co-oximeter

33
Q

How do you treat CO poisoning?

A

-100% O2 until COHgb level < 5% or for 6 hours
-Hyperbaric O2 therapy debatable

34
Q

How does Hydrogen Cyanide poisoning occur?

A

HCN poisoning is produced by the combustion of plastics, foam, paints, wool, and silk.
-Binds terminal cytochrome on the electron transport chain blocking the intracellular use of O2

35
Q

What are the S/Sx of Hydrogen Cyanide poisoning?

A

-Hypoxia, lactic acidosis, elevated mixed venous saturation
-loss of consciousness, dilated pupils, seizures, hypotension, and tachypnea followed by apnea

36
Q

What is the half-life of Hydrogen Cyanide?

A

1 hour (!)

37
Q

What is the treatment for Hydrogen cyanide poisoning?

A

-Hydroxocobalamin (Vit B12a)
-Binds cyanide forming cyanocobalamin with direct renal excretion.